The NF-κB pathway has been proposed to provide a link between inflammation and carcinogenesis. NF-κB signalling is activated by various stress-associated stimuli such as pathogen associated molecular patterns (PAMPs), inflammatory cytokines and UV-light. Since NF-κB activation induces the expression of anti-apoptotic molecules, proinflammatory mediators and anti-microbial peptides, it is a central regulator of inflammatory processes. Moreover, various cancers exhibit increased activation of NF-κB, not only in tumour infiltrating immune cells, but also in cancer cells themselves. In tumour cells NF-κB is believed to act mainly to prevent tumour cell death and promote proliferation, whereas in immune cells NF-κB functions to induce secretion of cytokines and growth factors to sustain tumour growth and angiogenesis. However, so far it has not been addressed whether activation of NF-κB signalling is sufficient to initiate tumour development through cell-intrinsic tumourpromoting effects in pre-malignant cells. Here we show that expression of constitutively active IKK2, the central kinase inducing canonical NF-κB activation,specifically in intestinal epithelial cells of mice results in spontaneous inflammation of the colon and the small intestine. Constitutive activation of IKK2/NF-κB in the intestinal epithelium induced recruitment and activation of inflammatory cells and stromal fibroblasts. Furthermore, expression of IKK2ca in the intestinal epithelium rendered mice more susceptible to DSS-mediated colitis and strongly enhanced tumour development in chemically induced and Apc-mutation mediated tumourigenesis. IKK2ca-expressing IECs exhibited increased proliferative activity,stabilisation of β-catenin and elevated expression levels of stem cell associated factors. Importantly, expression of IKK2ca in intestinal epithelial cells was sufficient for spontaneous tumour development, both in the colon and the small intestine of aged mice.Therefore results presented in this thesis imply that constitutive activation of IKK2/NF-κB in the intestinal epithelium is sufficient to promote and induce intestinal tumourigenesis through cell-intrinsic mechanisms, as well as through creating a tumour-promoting, inflammatory microenvironment.